Abstract

Penile erection is a neurovascular process controlled by numerous tightly regulated events, and occurs in response to the activation of pro-erectile autonomic pathways. It is dependent on an adequate inflow of blood to the erectile tissue through both endothelium-dependent vasodilatation and corporal smooth muscle relaxation. Pathologic alteration in the endothelium of penile vasculature and/or erectile tissue and/or impairment of neurovascular processes can result in erectile dysfunction (ED). Both cardiovascular disease (CVD) and ED have been linked to endothelial dysfunction. Endothelial dysfunction is a vascular condition resulting in a diminished vasodilatory response to pharmacologic and physiologic stressors. Endothelial dysfunction may be a pathophysiologic mechanism underlying both ED and CVD, forming a unifying link between these two conditions. Furthermore, in the general population and in men with diabetes or obesity, ED may be a valuable early marker for serious subclinical CVD, coronary artery disease and atherosclerosis.

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